The involvement of glutamate in recall of the conditioned NK cell response

Kuo, Jon‐Son; Chen, Sung Fang; Huang, Hsin‐Yu; Yang, Chung‐Shi; Tsai, Perng Jy; Hsueh, Chi-Mei

doi:10.1016/s0165-5728(01)00340-x

Cited by 30 publications

(13 citation statements)

References 50 publications

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“…As a matter of fact, platelets have been shown to possess NMDA receptors, which may play an antiaggregating role on activation (Franconi et al, 1996). Additionally, glutamate might be involved in modulating the functions of white blood cells (Kuo et al, 2001), possibly playing a role in the interaction between platelets and leukocytes at the level of the tissue injury. Moreover, human cerebral endothelial cells have been shown to express functional NMDA receptors, the stimulation of which, theoretically after glutamate release, may lead to breakdown of the blood-brain barrier (Sharp et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, a putative role for glutamate in modulating the functions of blood cells has already been proposed. In fact, platelets (Franconi et al, 1996), white blood cells (Kuo et al, 2001), and endothelial cells (Sharp et al, 2003) express functional NMDA receptors, suggesting that they are possible peripheral targets for glutamate released into the circulation.…”

Section: Introductionmentioning

confidence: 99%

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Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Aliprandi

Longoni

Stanzani

et al. 2005

J Cereb Blood Flow Metab

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Experimental studies have shown the role of excitotoxicity in the pathogenesis of ischemic brain lesions, and glutamate levels have been found to be elevated in CSF and plasma from patients, early after stroke. In this study, we investigated whether platelets could be involved in the mechanism of altered plasma glutamate levels after stroke. Forty four patients, from 6 hours to 9 months after ischemic stroke, 15 age-related healthy controls and 15 controls with stroke risk factors or previous transient ischemic attack were enrolled. Glutamate plasma levels, platelet glutamate release after aggregation and platelet glutamate uptake were assessed. Plasma glutamate levels were increased up to 15 days after the ischemic event in stroke patients, and the levels at day 3 were inversely correlated with the neurologic improvement between day 3 and 15. Ex vivo platelet glutamate release was decreased by 70% in stroke patients, suggesting previous in vivo platelet activation. Moreover, platelet glutamate uptake in these patients was decreased by 75% up to 15 days and was still reduced 90 days after stroke. Our data show a prolonged increase of glutamate in plasma after stroke, which might presumably be linked to altered platelet functions, such as excessive release of the amino acid or impaired uptake.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Aliprandi

Longoni

Stanzani

et al. 2005

J Cereb Blood Flow Metab

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show abstract

“…The content of glutamate was measured using the high performance liquid chromatography (HPLC) technique as previously reported (Kuo et al, 2001). For the determination of glutamate release, cells were seeded onto 24-well plates at a density of 2 3 10 5 cells/well.…”

Section: Glutamate Measurementmentioning

confidence: 99%

Glutamate released by Japanese encephalitis virus‐infected microglia involves TNF‐α signaling and contributes to neuronal death

Chen

Chang

et al. 2011

Glia

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The substantial activation of microglia in Japanese encephalitis virus (JEV)-induced Japanese encephalitis found in numerous studies demonstrates that the disease pathogenesis involves bystander damage caused by microglia-released mediators. Previously, we reported that microglia synthesized and secreted bioactive mediators with neurotoxic potential into the cultured supernatants in response to JEV infection. In this study, we found that the supernatants of JEV-infected microglia caused MK801-inhibitable neuronal damage in cultured neurons, indicating a potential excitotoxic mechanism. Infection with JEV was found to elicit the extracellular glutamate accumulation from microglia but not from neuron and astrocyte cultures. The glutaminase inhibitor 6-diazo-5-oxo-L-norleucine, cystine/glutamate antiporter inhibitor α-aminoadipic acid, and the gap junction inhibitor carbenoxolone reduced JEV infection-induced microglial glutamate release and neurotoxicity. We further demonstrated that tumor necrosis factor-alpha (TNF-α) was a key cytokine which stimulated extensive microglial glutamate release by up-regulating glutaminase expression via signals involving protein kinase C, cAMP responsive element-binding protein, and CAAT-enhancer-binding protein-beta. Although the elevated expression of excitatory amino acid transporter 1 and 2 was observed in JEV-infected cells, the glutamate uptake activity was significantly inhibited by TNF-α. The JEV infection-induced alterations, such as the extracellular glutamate release and glutamate-mediated excitoneurotoxicity, also occurred in neuron/glia cultures. Our findings support a potential link between neuroinflammation and the development of excitotoxic neuronal injury in Japanese encephalitis. The link between neuroinflammation and excitotoxic death may involve a mechanism in which TNF-α released by microglia plays a facilitory role in glutamate excitoneurotoxicity via up-regulation of glutamate synthesis and down-regulation of glutamate uptake.

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“…Thus far, however, only a limited number of studies have attempted to analyze the central mechanisms responsible for the conditioning of immune functions (Ramírez-Amaya et al, 1996Hsueh et al, 1999Hsueh et al, , 2002Ramírez-Amaya and Bermú dezRattoni, 1999;Kuo et al, 2001;Chen et al, 2004). Apart from these observations, no systematic approach has been undertaken to elucidate the neural processes underlying conditioning of immune functions.…”

Section: Introductionmentioning

confidence: 99%

Neural Substrates for Behaviorally Conditioned Immunosuppression in the Rat

Pacheco-López¹,

Niemi²,

Kou³

et al. 2005

J. Neurosci.

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We have previously demonstrated behaviorally conditioned immunosuppression using cyclosporin A as an unconditioned stimulus and saccharin as a conditioned stimulus. In the current study, we examined the central processing of this phenomenon generating excitotoxic lesions before and after acquisition to discriminate between learning and memory processes. Three different brain areas were analyzed: insular cortex (IC), amygdala (Am), and ventromedial nucleus of the hypothalamus (VMH). The results demonstrate that IC lesions performed before and after acquisition disrupted the behavioral component of the conditioned response (taste aversion). In contrast, Am and VMH lesions did not affect conditioned taste aversion. The behaviorally conditioned suppression of splenocyte proliferation and cytokine production (interleukin-2 and interferon-␥) was differentially affected by the excitotoxic lesions, showing that the IC is essential to acquire and evoke this conditioned response of the immune system. In contrast, the Am seems to mediate the input of visceral information necessary at the acquisition time, whereas the VMH appears to participate within the output pathway to the immune system necessary to evoke the behavioral conditioned immune response. The present data reveal relevant neural mechanisms underlying the learning and memory processes of behaviorally conditioned immunosuppression.

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The involvement of glutamate in recall of the conditioned NK cell response

Cited by 30 publications

References 50 publications

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Increased Plasma Glutamate in Stroke Patients Might Be Linked to Altered Platelet Release and Uptake

Glutamate released by Japanese encephalitis virus‐infected microglia involves TNF‐α signaling and contributes to neuronal death

Neural Substrates for Behaviorally Conditioned Immunosuppression in the Rat

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